Journal
SAUDI PHARMACEUTICAL JOURNAL
Volume 25, Issue 4, Pages 595-600Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jsps.2017.04.029
Keywords
GRP78; Endoplasmic reticulum stress; Mitochondrion; TSA
Categories
Funding
- Science and Technology Key Project in Jilin Province of China [2013-088]
- Natural Science Foundation of China [81570253]
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Endoplasmic reticulum stress (ERS) activates an adaptive unfolded protein response (UPR) that facilitates cellular repair, however, under prolonged ER stress, the UPR can ultimately trigger apoptosis thereby terminating damaged cells. Recently, TSA has shown protective effects on ERS and its mechanisms related to ER pathway has been previously characterized. However, whether TSA exerts its protective role via metabolic events remain largely undefined. Objectives: To explore the possible involvement of the metabolic changes during ERS and to better understand how TSA influence mitochondrial function to facilitate cellular adaptation. Results: TSA is an inhibitor of histone deacetylase which could significantly inhibit H9c2 cell apoptosis induced by Thapsigargin (TG). It also intervene the decrease of mitochondrial membrane potential. By immunofluorescence staining, we have shown that GRP78 was concentrated in the perinuclear region and co-localized with ER. However, treatments with TG and TSA could let it overlap with the mitochondrial marker MitoTracker. Cellular fractionation also confirmed the location of GRP78 in mitochondrion. Conclusions: TSA decreases ERS-induced cell apoptosis and mitochondrial injury may related to enhance the location of GRP78 in mitochondrion. (C) 2017 The Authors. Production and hosting by Elsevier B.V. on behalf of King Saud University.
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